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慢性高碳酸血症期间尿PCO2作为集合管氢离子分泌指标

Urinary pCO2 as an index of collecting duct hydrogen ion secretion during chronic hypercapnia.

作者信息

Batlle D C, Schlueter W, Foley R, Kurtzman N A

出版信息

Miner Electrolyte Metab. 1985;11(4):230-9.

PMID:2993836
Abstract

The rise in urinary pCO2 above blood pCO2 which occurs in response to bicarbonate loading (i.e. the urine to blood (U-B) pCO2 gradient), is used with increasing frequency as an index of collecting duct hydrogen ion secretion. We recently proposed, however, that the U-B pCO2 gradient is not an appropriate index of collecting duct hydrogen ion secretion when blood pCO2 is altered acutely. This issue was further investigated by examining the effect of chronic hypercapnia on urinary pCO2 generation. In rats exposed to chronic hypercapnia induced by breathing 10% CO2 for 3 days in an environmental chamber, acute sodium bicarbonate infusion resulted in a U-B pCO2 lower than that of normocapnic control rats (11 +/- 4.6 and 30 +/- 1.8 mm Hg, p less than 0.001). This finding could be interpreted to indicate that collecting duct hydrogen ion secretion is depressed in rats with chronic hypercapnia. The urinary pCO2 of rats with chronic hypercapnia was lower than that of the blood (54 +/- 6.0 and 86 +/- 1.2 mm Hg, p less than 0.005, respectively). In these rats, NaHCO3 infusion, while blood pCO2 was kept constant, elicited a marked rise in urine pCO2 (from 54 +/- 6.0 to 104 +/- 6.0 mm Hg, p less than 0.005) which was not significantly different from that observed in normocapnic control rats. The infusion of carbonic anhydrase resulted in a comparable fall in urine pCO2 in hypercapnic and normocapnic rats (-27 +/- 5 and -30 +/- 3 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

因碳酸氢盐负荷而出现的尿PCO₂高于血PCO₂的情况(即尿与血(U-B)的PCO₂梯度),越来越频繁地被用作集合管氢离子分泌的指标。然而,我们最近提出,当血PCO₂急性改变时,U-B PCO₂梯度并非集合管氢离子分泌的合适指标。通过研究慢性高碳酸血症对尿PCO₂生成的影响,对这一问题进行了进一步调查。在环境舱中呼吸10% CO₂ 3天诱导产生慢性高碳酸血症的大鼠中,急性输注碳酸氢钠导致U-B PCO₂低于正常碳酸血症对照大鼠(分别为11±4.6和30±1.8 mmHg,p<0.001)。这一发现可解释为表明慢性高碳酸血症大鼠的集合管氢离子分泌受到抑制。慢性高碳酸血症大鼠的尿PCO₂低于血PCO₂(分别为54±6.0和86±1.2 mmHg,p<0.005)。在这些大鼠中,在血PCO₂保持恒定的情况下输注NaHCO₃,引起尿PCO₂显著升高(从54±6.0至104±6.0 mmHg,p<0.005),这与正常碳酸血症对照大鼠中观察到的情况无显著差异。输注碳酸酐酶导致高碳酸血症和正常碳酸血症大鼠的尿PCO₂出现类似下降(分别为-27±5和-30±3 mmHg)。(摘要截断于250字)

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